These studies are based on the hypothesis that central neural mechanisms are more important in the regulation of respiration in the newborn than traditionally recognized. We use an animal model which eliminates the confounding effects of changes in blood gases which occur during change in respiratory drive. Mixed breed piglets and lambs, two through seven days of age, are anesthetized, gallamine paralyzed and mechanically ventilated. An electronic circuit was constructed which servo-controls the rate of a volume mechanical ventilator keeping end-tidal PCO2 constant. Respiratory output is quantified by moving average of phrenic neural acitivity. This is done with a specially constructed active filter (Butterworth) which has a rise time-constant of 50ms. We found that persistent apnea and prolonged respiratory inhibition follow offset of apnea producing electrical stimulation of the superior laryngeal nerve. Vagal stimulation also caused apnea but was not associated with prolonged respiratory inhibition. These results indicate that superior laryngeal nerve stimulation excites a central neural mechanism which serves to prolong respiratory inhibition beyond stimulus offset. We have found also that chemical drive due to CO2 acts in opposition to the inhibitory SLN mechanism suggesting subthreshold respiratory modulation by this afferent input. Finally, we have shown that poststimulus carotid sinus nerve induced respiratory activity is independent of poststimulus superior laryngeal nerve inhibition, suggesting independece of these two afterdischarge mechanisms.